Social cognition impairments after aneurysmal subarachnoid haemorrhage: Associations with deficits in interpersonal behaviour, apathy, and impaired self-awareness

- Aspects of social cognition (emotion recognition, ToM, and empathy) were impaired post-aSAH.
- Social cognition deficits were associated to behavioural disturbances after aSAH.
- An association between impaired self-awareness and deficits in social cognition was found.
- Social cognitive deficits were not related to lesion location on MRI or aneurysm circulation.

Behavioural disturbances are frequently found after aneurysmal subarachnoid haemorrhage (aSAH). Social cognition impairments have been suggested as a possible underlying mechanism for behavioural problems. Also, aSAH is likely to result in damage affecting frontal-subcortical circuits underlying social cognition. Therefore, we aimed to investigate social cognition after aSAH and its associations with behavioural problems (deficits in interpersonal behaviour, apathy, and impaired self-awareness) and focal as well as diffuse brain damage. 88 aSAH patients (in the subacute phase post-aSAH) and 60 age-, sex- and education-matched healthy controls participated. Tasks for emotion recognition, Theory of Mind (ToM), and empathy as well as questionnaires were used. Cortical infarctions in frontal and non-frontal areas on MRI, aneurysm circulation and aSAH-related events were taken into account. Compared to healthy controls, aSAH patients performed significantly worse on tasks for emotion recognition, ToM and empathy. Poor performance on ToM and emotion recognition was associated with proxy-ratings indicating impaired interpersonal behaviour and apathy and with indications of impaired self-awareness. No associations were found between deficits in social cognition and frontal or non-frontal cortical lesions on MRI. Also, aneurysm circulation and aSAH-related events such as hydrocephalus, vasospasm, and treatment method did not explain why and how social cognitive deficits did occur after aSAH. In conclusion, emotion recognition, ToM and empathy were clearly impaired in aSAH patients and these deficits were related to apathy and deficits in interpersonal behaviour as reported by proxies and to impaired self-awareness. This association strengthens the assumption of impaired social cognition as an underlying construct of behavioural problems after aSAH. Consequently, social cognition tests and proxy-ratings should be used in clinical practice, irrespective of lesion location on MRI or aneurysm circulation, to improve the detection and treatment of apathy and deficits in interpersonal behaviour after aSAH.